There are multiple approaches for controlling a pacing rate of a rate-adaptive pacemaker to provide a heart rate adequate to meet the metabolic demand (J. G. Webster, Design of Cardiac Pacemaker. Piscataway, N.J.: IEEE Press, 1995.). Different sensors have been used to assess metabolic demands (workload of the body WBody), including body acceleration and movement activity and transthoracic bioimpedance to estimate minute volume MV (see also FIG. 1). Minute ventilation, the product of breathing rate and tidal volume, correlates well with workload Wbody. An ideal rate-adaptive pacing system would automatically control upper and lower rate limits to prevent over pacing (M. Min, A. Kink, T. Parve, “Rate adaptive pacemaker,” U.S. Pat. No. 6,885,892, Apr. 26, 2005.) and under pacing (M. Min, A. Kink, T. Parve, “Rate adaptive pacemaker using impedance measurements and stroke volume calculations,” U.S. Pat. No. 6,975,903, Dec. 13, 2005). These patents are incorporated herein by reference for all purposes.
Over pacing can take two forms. In the first form, the paced heart rate is too high for normal ventricular filling (under filling phenomenon takes place), putting the heart on the descending limb of the Starling curve and resulting in a decrease in cardiac output CO=SV·PR (see FIG. 1 and FIG. 2, where SV is a stroke volume), though the pacing rate PR goes higher. In the second form, an adequate cardiac output is maintained but the heart rate, and therefore the cardiac oxygen consumption, is greater than necessary to supply overall metabolic demand of myocardium. This can promote cardiac ischemia and, potentially, arrhythmias.
The under pacing phenomenon occurs when the sensed demand is low (e.g., during a deep sleep) and the paced heart rate is either insufficient to meet metabolic demand or the cardiac output is maintained primarily by increasing a preload (i.e., increasing end-diastolic volume and stroke volume) (U.S. Pat. No. 6,975,903). This situation was common in the early days of fixed-rate pacing. The accompanying increases in wall-stress can promote hypertrophy, fibrosis and heart failure.
The heart rate is critical because it is possible for metabolic demand to exceed the capabilities of the damaged heart. The artificial pacing system may drive the heart into failure while trying to meet the metabolic demand. Traditionally, the upper and lower pacing rate limits to avoid over and under pacing of the heart are determined by the implanting physician and are programmed into the pacemaker at the time of implanting the device. The actual values may be determined from exercise studies, from algorithms which take into account patient's characteristics, or from clinical experience and are set for every patient individually (Webster, above).
Incorrect rate limits or rate response can have serious impact on a patient's quality of life. For example, postural hypotension, a sudden drop in blood pressure caused by shifts in blood volume to the lower extremities due to a decrease in hydraulic resistance, Rbody (FIG. 1), when rising from a seated or supine posture, can lead to syncope and falling of the patient, or worse. Neurogenic syncope is a similar problem but even more insidious because the sudden drop in blood pressure may occur minutes after the precipitating event.
If the normal compensatory vasoconstriction is missing or remains insufficient, the condition may be ameliorated by increasing the heart rate. Obviously, the timing and the extent of the heart rate increase are important.
Patient's upper rate limit is determined by the following factors. The ability of heart to work at higher rates is correlated with a better coronary reserve (CR), characterized with a capability to dilate coronary arteries and, therefore, to reduce the hydraulic resistance R of the myocardium (FIG. 1). Myocardium damaged during an ischemic event or by other disease (e.g., diabetes) has limited cardiac reserve and capability to cope with the rising cardiac demand W.
The ability to operate at low heart rates is determined by the ability of the heart to supply adequate cardiac output at rest, COrest=SVrest·PRrest (FIG. 1 and FIG. 2). Here the limitations occur during ventricular filling. A compliant heart with good diastolic function is able to increase end-diastolic volume with minimal increase in filling pressure and can double stroke volume, and therefore cardiac output, without a rate increase. This over filling phenomenon is accompanied by an increase in myocardial “stretch” and wall stress (see U.S. Pat. No. 6,975,903).
It is critical to maintain a balance between an energy demand W and a supply E in the heart (FIG. 1). Since insufficient myocardial perfusion will lead to hypoxia, ischemia, and infarct, under most circumstances the primary concern must be to maintain adequate cardiac perfusion and to guarantee that W is less than or equal to E.
A myocardial energy imbalance is determined as follows. Useful energy consumption, i.e., the external work W of the myocardium during a cardiac cycle can be characterized by the stroke work, the area Sdem of the pressure-volume loop (PV-loop), which characterizes the relationship between ventricular volume V and ventricular pressure P, as shown in FIG. 3a. On the other hand, the energy supply E is proportional to the pressure difference between the aortic (or arterial) and ventricular pressure over the duration of diastole tdiast (FIG. 2 and FIG. 3b). Therefore, the energy supply E is proportional to the area Ssup in FIG. 2b. 
More precisely, Sdem is the external work done by the ventricle during a cardiac cycle tcycle=tdiast+tsyst (see FIG. 2) for pumping blood into the aorta (A. B. Ericsson, Cardioplegia and Cardiac Function Evaluated by Left Ventricular P-V Relations, PhD.thesis, Karolinska Institutet, Stockholm, Sweden, Stockholm, 2000. ISBN 91-628-4138-6; E. Söderqvist, Left ventricular volumetry technique applied to a pressure guide wire, Licentiate thesis, Royal Institute of Technology, Stockholm, Sweden, 2002. ISBN 91-7283-318-1). However, an additional work is required for storing potential energy into myocardium (cocking of myocardium's fibers). This is called an internal static work and is proportional to the roughly triangular area Spot in FIG. 4. Thus, the energy supply E to the myocardium must be slightly greater than or equal to the energy consumed by the myocardium for both the external dynamic work, i.e., for pumping blood into a vascular system, and the internal static work of the myocardium.
Therefore, there is a need for a device and a method that takes the internal static work into account when determining the myocardial energy balance.
FIG. 4 shows that blood pressure must be measured to determine both Spot, proportional to the internal static work, and Sdem, proportional to the external work. However, constant measuring of blood pressure can be complex task.
Therefore, there is a need for a device and a method that determines the myocardial energy balance without the need for blood pressure measurements.